Alternative polyadenylation of Pax3 controls muscle stem cell fate and muscle function

Author:

de Morree Antoine12ORCID,Klein Julian D. D.12,Gan Qiang12ORCID,Farup Jean123ORCID,Urtasun Andoni12,Kanugovi Abhijnya12,Bilen Biter12ORCID,van Velthoven Cindy T. J.12ORCID,Quarta Marco124,Rando Thomas A.124ORCID

Affiliation:

1. Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.

2. Paul F. Glenn Center for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA.

3. Departments of Clinical Medicine and Biomedicine, Research Laboratory for Biochemical Pathology, Aarhus University, Aarhus, Denmark.

4. Center for Tissue Regeneration, Repair, and Restoration, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA.

Abstract

Skeletal muscle during homeostasis Muscle stem cells function in the regeneration of skeletal muscle after injury, but their role in homeostasis is unclear. De Morree et al. show that, in the absence of injury, stem cells in different muscles have different rates of spontaneous activation and fusion, which depend on the level of Pax3 protein (see the Perspective by Xi and Pyle). Regulation of Pax3 protein occurs posttranscriptionally through the small nucleolar RNA U1 and microRNA miR206. This work explains how muscle stem cells are maintained under normal conditions and shows that homeostatic muscle stem cell activation varies in different muscle groups. Science , this issue p. 734 ; see also p. 684

Funder

National Institutes of Health

U.S. Department of Veterans Affairs

Glenn Foundation for Medical Research

Muscular Dystrophy Association

FSH Society

Lundbeckfonden

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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